Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pneumatic dilatation of the cardia is an effective procedure to treat patients suffering from achalasia. Eighty percent of these patients can be expected to have excellent or good results for 6 years after the first dilatation. A repeat dilatation should be performed as soon as the patient has recurrent symptoms, usually every 2 years. Calcium channel blockers (nifedipine and verapamil) or nitrates (isosorbide dinitrate) decrease LES pressure but do little to the clinical symptomatology of patients with achalasia; however such drug therapy may be tried as an adjunct in patients who remain symptomatic after pneumatic dilatations or myotomy. Pneumatic dilatation and surgical myotomy both reduce LES pressure; with pneumatic dilatation, enough residual LES pressure is retained to prevent gastroesophageal reflux. Indeed, reflux esophagitis seems to occur more often after surgery than after forceful dilatations. We think that pneumatic dilatation should be performed as the primary therapy and surgery reserved for the failures of this procedure.
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PMID:Non-surgical management of achalasia. 163 43

In about 50% of the cases, non-cardiac chest pain is due to hypomotile or hypermotile functional disorders of the esophagus. X-ray examination, endoscopy and manometry, possibly with provocation with edrophonium, confirm the diagnosis. Gastro-esophageal reflux is found in 40%, motility disorders in 20%, and an irritable esophagus in 40% of the cases. For diagnosis ex juvantibus, gastroprokinetic drugs or H2-blockers, nitro compounds and calcium antagonists may be useful.
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PMID:[Non-cardiac thoracic pain. Diagnosis, differential diagnosis and therapy]. 202 80

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.
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PMID:Rational pharmacotherapy of gastrointestinal motility disorders. 266 4

Various oesophageal manometric disorders have been associated with chest pain or dysphagia. The classic motility disorders are achalasia and diffuse oesophageal spasm. In achalasia, a disorder of aperistalsis in the oesophageal body and incomplete relaxation of the lower oesophageal sphincter, either surgical myotomy or pneumatic dilatation is an effective approach, although some investigators have suggested a role for pharmacological therapy. For the treatment of diffuse oesophageal spasm, a disorder of non-peristaltic motor activity in the oesophagus, various pharmacological approaches with nitrates, anticholinergics, and calcium antagonists have been used. In the presence of associated lower oesophageal sphincter dysfunction, bouginage or pneumatic dilatation may be indicated. Long oesophagomyotomy should be considered for those patients who fail to respond to these measures. Recent manometric techniques have led to the identification of patients with chest pain or dysphagia who have abnormalities of increased contractile amplitude ('nutcracker' oesophagus) or duration. An association with gastro-oesophageal reflux or with psychiatric disturbance has been suggested. Treatment directed towards these factors is indicated and may be supplemented by pharmacological intervention, e.g. by calcium antagonists or anticholinergics.
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PMID:Primary oesophageal motility disorders. Current therapeutic concepts. 286 26

Calcium-channel blocking agents can relieve anginal and chest pain associated with hypermotility of the esophagus. Although calcium-channel antagonists differ in their effects on the esophageal body and the lower esophageal sphincter, reduction of lower esophageal sphincter pressure theoretically could result in gastroesophageal reflux and pain. This pain may be difficult to differentiate from chest pain of cardiac origin. An association between calcium-channel blocking agents and chest pain is speculative at this time. However, the possibility of such an effect should be considered by clinicians in the total management of patients. Future clinical studies are warranted to address the issue of the incidence of such an effect and to define more precisely the potential interrelationship among the calcium-channel antagonists, their efficacy in relieving cardiac pain, and their potential liability in inducing chest pain of noncardiac origin.
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PMID:Calcium-channel blocking agents and chest pain. 304 91

Esophageal motility disorders consist of a complex array of disturbances in normal esophageal function associated with dysphagia, gastroesophageal reflux, and noncardiac chest pain. A thorough knowledge of normal esophageal anatomy and physiology is important to a full understanding of these motility derangements. Through a complicated interaction of neuromuscular and hormonal influences, the voluntary act of swallowing transforms into an automated sequence of peristaltic waves propelling food and liquids into the stomach in concert with coordinated relaxation of the sphincters. Anatomic and physiologic barriers exist within the esophagus protecting against gastroesophageal reflux and aspiration. With improvements in diagnostic tools such as barium contrast radiography, scintigraphy, pH measurements, and esophageal manometrics with provocative testing, motility disorders have become better defined and understood. Primary motility disorders consist of achalasia, diffuse esophageal spasm (DES), "nutcracker esophagus," hypertensive lower esophageal sphincter, and nonspecific esophageal motility dysfunction (NEMD). A host of secondary and miscellaneous motility disorders also affect the esophagus, including scleroderma and other connective tissue diseases, diabetes mellitus, Chagas' disease, chronic idiopathic intestinal pseudo-obstruction, and neuromuscular disorders of striated muscle. Gastroesophageal reflux disease (GERD) may also be promoted by associated motility disturbances. Treatment modalities include surgical myotomy; dilatation; and pharmacologic manipulations, including use of nitrates, calcium-channel blockers, H2-blockers, and psychotropic drugs where appropriate.
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PMID:Esophageal motility disorders. 329 77

Gastroesophageal reflux is a common event during infancy. Developmental factors may be responsible for incompetence of the lower esophageal sphincter (LES) in this age group. We used the cat as a model to evaluate in vivo and in vitro the mechanical factors responsible for LES pressure during infancy. We found that in vivo the kitten develops lower LES pressure than the adult cat. For in vitro studies consecutive rings 1.75 mm wide were obtained from the LES region of 3-day-, 1-wk-, 3-wk-, and 6-wk-old kittens and of adult animals. Force-length curves were obtained in standard Tyrode's solution, in Tyrode's solution with high KCl, and in calcium-free Tyrode's solution with ethylenediaminetetraacetic acid disodium salt to determine basal, total, and passive forces, respectively. Active force is given by the difference between total and passive force. The maximum active force generated was lowest in the 3-day-old kittens and increased with age, being highest in the adult cat. Stresses, obtained by normalizing forces for the amount of muscle available, were greater in the kitten than the adult. The ratio of muscle thickness to its inner radius is markedly reduced in the kitten. As intraluminal or LES pressure is given by the product of stress and thickness-to-radius ratio, this might explain why lower pressures are generated despite the higher stresses developed.
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PMID:Developmental characteristics of the lower esophageal sphincter in the kitten. 402 56

Disorders of swallowing in a given patient can result from abnormalities of dentition, the oral cavity (mouth and pharynx), the cricopharyngeal muscle, esophageal skeletal (proximal) or smooth (distal) muscle, the lower esophageal sphincter, and the stomach. Recent advances include refinements in esophageal manometric techniques with reclassification of motility disorders; newer drugs to treat gastroesophageal reflux; recognition of more frequent infections of the esophagus in immunosuppressed patients; and adaptation of the use of medications such as nitrates and calcium-channel blockers, which were previously primarily cardiotonic, for investigative treatment of esophageal motility abnormalities.
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PMID:Medical management of disorders of swallowing. 651 62

A case of milk-alkali syndrome is described in a 34-year-old man taking an over-the-counter antacid preparation for gastroesophageal reflux. A Tc-99m MDP bone scan performed in the initial investigation of the hypercalcemia was markedly abnormal with a "metabolic" pattern of tracer uptake similar to that seen in hyperparathyroidism and humoral hypercalcemia. Following withdrawal of the antacid and calcium, the bone scan appearance returned to normal, as did the biochemical markers of his disease.
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PMID:Increased skeletal uptake of Tc-99m methylene diphosphonate in milk-alkali syndrome. 803 69

Swallowing is a complex mechanism that is based on the coordinated interplay of tongue, pharynx, and esophagus. Disturbances of this interplay or disorders of one or several of these components lead to dysphagia, non-cardiac chest pain, or regurgitation. The major esophageal motility disorders include achalasia, diffuse esophageal spasm, hypercontractile esophagus ("nutcracker esophagus"), and hypocontractile esophagus ("scleroderma esophagus"). Other esophageal diseases such as hypopharyngeal (Zenker's) diverticula or gastroesophageal reflux disease also may be sequelae of primary esophageal motility disorder. Finally, a substantial group of patients referred for evaluation of possible esophageal motor disorders have milder degrees of dysmotility--referred to as nonspecific esophageal motor disorder--that are of unclear clinical significance. Medical treatment of esophageal motility disorders involves the uses of agents that either reduce (anti-cholinergic agents, nitrates, calcium antagonists) or enhance (prokinetic agents) esophageal contractility. Despite the beneficial effect of the various drugs on esophageal motility parameters, the clinical benefit of medical treatment is often disappointing. From clinical and epidemiological studies there is some evidence for a "psychological" component in the pathogenesis or perception of esophageal symptoms. Further understanding of esophageal pathophysiology, as well as development of new receptor selective drugs, might increase our chances of successful treatment of esophageal motility disorders.
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PMID:Medical treatment of esophageal motility disorders. 846 20


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